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30 Cards in this Set

  • Front
  • Back
venous drainage of adrenals
R- into IVC
L- into renal v
adrenal cortex produces
-cortisol (glucocorticoid)
-aldosterone (mineralcorticoid)
-testosterone (androgen)

epi & NE & DA
histo layers in adrenal
zona glomeruluosa (aldost)
zona fasiculata (cortisol)
zona reticularis (androgens)

medulla (epi & NE)
production of androgens
chol to pregnenolone
17 hydoxylase
(gives cortisol & DHEA)
DHEA to testosterone

(21 beta hydroxylase then 11 beta hydroxylase to cortisol)
production of cortisol
chol to pregnenolone (ACTH)
to 11 deoxycortisol (17 hydrox & 21 hydroxylase)
to cortisol (11 beta hydroxylase)
production of aldosterone
cholesterol to pregnenolone (AT II)
to progesterone
to 11 deoxycorticosterone (beta 21 hydroxylase)
to corticosterone (via 11 beta hydroxylase)
to aldosterone
congenital 17 alpha hydroxylase deficiency
excessive aldosterone
-HTN & hypokalemia

low androgen & low cortisol
-phenotypically female but no maturation
congenital 21 beta hydroxylase deficiency
low cortisol
-high ACTH

low aldosterone
-hypotension, hyponatremia
-high renin
-volume depletion & hypovolemic shock

excessive androgen
-female pseudohermaphroditism
congenital 11 beta hydroxylase
like 21 beta hydroxylase but Hypertension

(11 deoxycorticosterone is weak mineralcorticoid)
affects of cortisol
glucagon acts w/cortisol
activates aldosterone R when excess
feedback inhibition of ACTH

(suppress insulin, bone growth, immune system
increase blood pressure)
common glucocorticoids
hydrocortisone- cortisol

prednisolone & prednisone-
-activated by 11 hydroxylase
-tx inflammation

-tried for increased performance
-no intrinsic activity
-liver & kidney activate

-long biol activity on receptor
adrenal insufficiency (eg's)
primary= Addison's
secondary = pituitary tumor
tertiary= hypothalamic effect
mech of Addison's
adrenal gland damaged
lose feedback
elevated ATCH
mech of secondary AI
pituitary tumor
-adrenal gland atrophy
-low ATCH
mech of tertiary AI
hypothalamic defect
-b/c prednisone
-pit & HT suppressed
-lasts up to a year
fatigue, malaise, anorex
Lab: hypoNa, hyperK, acid, low glucose, eos, low Ca, azotemia
primary AI
mostly autoimmune
-AIDS, ALD, CAH, fungal, TB

get elevated ACTH

(think JFK)
active form glucocorticoid
(activated by 11 beta oxoreductase)

(inactivate to cortisone by 11 beta DH)
11 beta oxo-reductase
converts (activates) cortisone to cortisol
11 beta dehydrogenase
converts (inactivates cortisol to cortisone)
normal mineralcorticoid
low glucocort & androgen

ACTH stim test
Insulin Tolerance test
Metyrapone test
secondary AI

decreased ACTH
stim test many false neg

give emperical GC rplct if hypotensive
first line lab test for AI
NOT random cortisol

-primary AI <10
-may be low in secondary b/c atrophy
f/u lab tests for AI

distinguish primary v. secondary via plasma ACTH
meaning of negative cosyntropin
chronic AI excluded

f/u w/ITT, ACTH & metyrapone
may be mild or secondary AI
features of adrenal crisis
(acute AI)
mimic sepsis

hypoten, CV collapse
fever, weak, apathy, confusion
dehydrat, hypoNa, hyperK
N, V, anorexia
diagnosis of acute AI
random cortisol
cosyntropin (if stable)
treat (if unstable or pos cosyntropin)

tx w/IV cortisol
high basal cortisol
high free cortisol
blunted response to cosyntropin
relative AI
examples of hyperaldosteronism
Primary Hyperaldosteronism
weight gain
moon facies
truncal obesity
buffalo hump
(thin skin, osteoporosis, amenorrhea, immune suppression)
Cushings Syndrome = hypercortisolism

caused by:
-Cushing's dz
-primary adrenal
-ectopic ACTH production
-chronic steroids
positive dexamethasone supression test
to test Cushing's

-low cortisol after low dose

ACTH producing tumor:
-high cortisol after low dose
-low cortisol after high dose (normal rspns)

Cortisone producing tumor
-high cortisol after low or high dose
types & cause
primary= Conn's syndrome
-aldost secreting tumor
-has LOW plasma renin

-renal artery stenosis, renal failure, CHF, cirrhosis or nephrotic syndrome
-has HIGH plasma renin